Canine Bacterial Keratitis – When Ulcers Go Bad

By November 14, 2018Articles

by Dr. Noelle La Croix, DVM, Dip. ACVO

Canine Bacterial Keratitis – When Ulcers Go Bad

The cornea is a transparent tissue lacking pigments, blood vasculature, and keratinized epithelia. These properties are essential for vision, but also make the cornea susceptible to infection. The tear film acts as a physical barrier to microrganisms, prevents microbial growth with lysozyme and lactoferrin, and provides nutrition to the corneal epithelium. The tear film is replenished by the lacrimal glands, adheres to the corneal epithelium via mucin of goblet cells, and reforms during blinking. Lipids, excreted by the meibomian glands, prevent tear film evaporation from the corneal surface.

Minor injuries and abrasions to the corneal epithelium are well tolerated. These superficial (non-infected) ulcerations drive corneal nerves to release neuropeptides that restore epithelial integrity, promote cellular proliferation, and encourage wound healing. Mitotic cells slide into and fill these epithelial defects. An entire corneal epithelium can regenerate in most species within 48 to 72 hours.

When the corneal stroma is injured (deep ulceration), a more complex process of repair is instigated. In the damaged stroma, proteolytic enzymes are produced by inflammatory cells, corneal epithelia, fibroblasts, and introduced microorganisms. Excessive degradation (melting) is naturally prevented by proteolytic inhibitors found within the cornea and tear film. Clinically introduced inhibitors (0.2% EDTA, 0.1% doxycycline, 10% N-acetylcysteine, and/or 100% fresh serum) can further reduce this proteolytic degradation of the cornea. If proteolysis is not adequately inhibited, the melting cornea can perforate in less than 24 hours.

The clinical treatment for any corneal ulceration begins with a thorough examination, including Schirmer tear testing, fluorescein staining, and tonometry. Trauma and other medical history should be considered. The eyelids are examined for trichiasis, distichia, and ectopic cilia. Eyelid margins are inspected for meibomianitis. All conjunctival surfaces are examined for foreign bodies. Palpebral responses are tested. Finally the depth of the ulceration is accessed and classified as superficial or stromal.

Most simple superficial (often traumatic) ulcerations will heal within 7 days. To prevent infection, these uncomplicated ulcers are most effectively treated with a topical triple antibiotic (neomycin, polymyxin B, and bacitracin).

Corneal indentations and depressions are indicative of deeper stromal ulcerations. These ulcerations are often associated with bacterial infections (bacterial keratitis). Clinical signs of bacterial keratitis include corneal edema, corneal stromal cell infiltration, corneal melting, and the loss of corneal stroma (Figure 1). Scrapings of the infected area should be cytologically examined and submitted for culture and sensitivity testing. These serious infections usually require referral to an ophthalmologist, and/or hospitalization for hourly antibiotic and antiprotease treatment. Antibiotics and other drugs are delivered via the tear film since the cornea lacks a blood supply. Therapeutic drug concentrations are difficult to sustain in dogs with their high tear film turnover rate.

Most dogs with bacterial keratitis are brachycephalic, and about half will show decreased tear production (< 15 mm/min). Many brachycephalic dogs are lagophthalmic and so poorly replenish the tear film by blinking. In these breeds, medial canthal trichiasis and distichia can both cause ulceration and inoculate bacteria within the tear film. Dogs with decreased tear production do not effectively remove and lyse bacteria from the corneal surface. In these cases, bacterial access to the corneal epithelium is also increased.

Staphylococcus intermedius (29%), beta-hemolytic Streptococcus spp. (17%), and Pseudomonas aeruginosa (21%) are the most common organisms found in cases of canine bacterial keratitis. Many bacteria contain at least one antibiotic resistance gene, so a prophylactic combination of antibiotics (e.g.; tobramycin/ciprofloxacin) is often prescribed.

Both superficial and stromal ulcerations should be re-evaluated within 48 hours of initial examination. Superficial ulcers can quickly develop stromal involvement requiring more aggressive therapy. The close monitoring of the ulcerated patient will help prevent corneal melting and loss of vision.


Figure 1: A melting corneal ulcer in the left eye of a Jack Russell Terrier. Photo credit: Laura Eppig.